Midterm Exam- Cardiac Flashcards
P wave
atrial depolarization by SA node first
QRS complex
ventricular depolarization by parkinje fibers
T wave
ventricular repolarization
PR interval
how long conduction takes from SA to AV node
0.12-0.2 seconds
sinus bradycardia
heart rate below 60bpm.
treat with anticholinergic like atropine
sinus tachycardia
heart rate above 100bpm.
treat with beta blocker
premature atrial contractions (PACs)
normal beat but SA node fires sooner.
early+ abnormal P wave.
Will feel palpitations.
Caused by hypoxia, stimulants, infection.
atrial fibrillation
irregular rhythm and rapid nondefinite P wave.
high risk for blood clots.
Treat w beta blockers or calcium channel blockers, antiarrhythmic, cardioversion to control heart rate.
atrial flutter
no P wave, “flutter wave”
sawtooth pattern btw narrow QRS
supraventricular tachycardia (SVTs)
regular rate but rapid, narrow QRS.
Can see heart beating outside of chest. Hypotension
Treat cause.
junctional escape
when using AV node instead of SA node.
40-60bpm.
absent or upside down P wave
premature ventricular contractions (PVCs)
bizarre QRS.
Appears different in everyone.
treat cause+symptoms (r/t MI, caffeine, hypoxia, electrolyte imbalance)
ventricular tachycardia
3 PVCs and rapid rate.
Will experience shortness of breath.
Usually hypo or hyperkalemia. No pulse= start defib and chest compressions.
Pulse= electrolyte replacement and antiarrhythmics.
ventricular fibrillation
no cardiac output, looks like squiggles.
Lethal, start defib and chest compressions.
1st degree heart block
prolonged PR interval
(0.2+ seconds)
due to delayed atrial depolarization
complete heart block
P waves and QRS are independent of eachother.
AV node is blocked completely. Will need a pace maker.
semilunar valves
pulmonic and aortic valves
atrioventricular valves
tricuspid and mitral valves
systemic circulation
sends oxygenated blood from left side of heart to tissues via aorta
pulmonic circulation
deoxygenated blood from right side of heart to the lungs
coronary circulation
coronary arteries fill with oxygenated blood during diastole
cardiac output
CO= HR x SV.
Normal= 4-8L/min at rest
stroke volume
volume of blood ejected from heart with each beat
low cardiac output
not enough blood being pumped to the body.
occurs with bradycardia
cardiac index
specific CO adjusted to pt’s body surface area
ejection fracture
percent of blood ejected by each contraction
normal= 55%+
factors determing cardiac output
contractility
heart rate
preload
afterload
preload
volume of blood in ventricles at end diastole/amount of venous return back to heart.
CVP=central venous pressure
afterload
resistance which the ventricles has to pump against to get blood out
increased afterload=
increased blood pressure
arterial blood pressure
CO x SVR
Pressure of blood placed on walls of arterial system.
systemic vascular resistance
force opposing movement of blood
mean arterial pressure
MAP- average pressure within arterial system.
Normal= 65+.
MAP= (systolic + 2xdiastolic) divided by 3
S1 heart sound
closure of AV at systole
S2 heart sound
closure of SV at diastole
S3 heart sound
heard w volume overload or valve regurgitation
“ventricular gallop”
S4 heart sound
with forceful atrial contraction from resistance of ventricular filling
murmur
turbulent flow
friction rub
scratching sound with pericarditis
normal total cholesterol
below 200
normal HDL
above 40
normal LDL
below 100
normal trigylcerides
below 150
need consent form for
cardiac cath lab
electrophys studies
troponin
lab value tested in chest pain
if elevated= MI
normal= less than 0.4
myoglobin
elevated in damage to heart but does not stay elevated for long
normal= 0-85
CKMB
lab value elevated in MI
normal= 0-3
CRP
C reactive protein in liver
elevated in any bodily inflammation
normally= 0
BNP
normal is less than 100 Elevated= heart failure
stress test
assess heart function under stress
if positive= go to cath lab
no caffeine or smoking before
NPO 4 hours prior
TEE
an echocardiogram
NPO 8 hrs prior
need sedation
bell of stethoscope
smaller side
better for high pitched sounds like S3 S4 murmurs
factors affecting arterial circulation
baroreceptors
chemoreceptors
SNS
PNS
baroreceptors
located in aortic arch and carotid sinus
will decrease heart rate and decrease vasodilation during hypervolemia
chemoreceptors
located in medulla
triggered in hypoxia or hypercapnea
acute respiratory failure
type 1: hypoxic
type 2: hypercapnic.
Give steroids and bronchodilators, admin oxygen.
Can lead to ARDS.
ARDS
acute respiratory distress syndrome
lack of perfusion from trauma. Treat w mechanical ventilation and corticosteroids.
Three phases: Exudative, proliferative, fibrotic.
exudative phase of ARDS
alveoli fill and collapse
will hear rale sounds
proliferative phase of ARDS
pulmonary hypertension
start of right sided heart failure
fibrotic phase of ARDS
scarring of worsened right sided heart failure
hypotension
flail chest
when 3+ ribs fractured
pneumothorax
collapsed lung
diminished/absent lung sounds
hemothorax
blood in lungs
tachycardia, tachypnea, sharp chest pain
tension pneumothorax
untreated pneumothorax
tracheal shift and blood vessels deviate
cardiac tamponade
excess fluid or air in pericardial sac
medical emergency
decreased CO and BP
tachycardia as compensation
antidote to coumadin
vitamin K
pulmonary embolism
clot in lung from DVT
give anticoagulant (heparin)
give thrombolytic (tPa)
send home on lovanox or coumadin
monitor for bleeding
if allergic to shellfish
give antihistamine
give steroid
give anti acid reflux
ST elevation
sign of MI
virchow’s triad
three causes for DVT
venoustasis
vessel damage
hypercoagulability
D dimer
elevated= blood clot
left sided heart failure
pushes back blood up to pulmonary system.
pulmonary edema, crackles, cyanosis, weak peripheral pulses, hypotension
right sided heart failure
blocks blood into circulation.
JVD, peripheral edema, ascites
beta blockers
decrease heart rate
reduce afterload
ace inhibitors
reduce fluid volume
reduce afterload
